Undernourished mice infected (UI) submitted to low and long-lasting infections by
Schistosoma mansoni are unable to develop the hepatic periportal
fibrosis that is equivalent to Symmers’ fibrosis in humans. In this report, the
effects of the host’s nutritional status on parasite (worm load, egg viability and
maturation) and host (growth curves, biology, collagen synthesis and characteristics
of the immunological response) were studied and these are considered as
interdependent factors influencing the amount and distribution of fibrous tissue in
hepatic periovular granulomas and portal spaces. The nutritional status of the host
influenced the low body weight and low parasite burden detected in UI mice as well as
the number, viability and maturation of released eggs. The reduced oviposition and
increased number of degenerated or dead eggs were associated with low protein
synthesis detected in deficient hosts, which likely induced the observed decrease in
transformation growth factor (TGF)-β1 and liver collagen. Despite the reduced number
of mature eggs in UI mice, the activation of TGF-β1 and hepatic stellate cells
occurred regardless of the unviability of most miracidia, due to stimulation by
fibrogenic proteins and eggshell glycoproteins. However, changes in the repair
mechanisms influenced by the nutritional status in deficient animals may account for
the decreased liver collagen detected in the present study.